Over the past decade, targeted therapy with tyrosine kinase inhibitors (TKIs) such as erlotinib or gefitinib and anaplastic lymphoma kinase inhibitors (ALK) such as crizotinib have improved clinical outcome in a subset of lung cancer patients whose tumors harbor EGFR (epidermal growth factor receptor) and EML4-ALK (echinoderm microtubule-associated protein-like 4 and anaplastic lymphoma kinase) alterations, respectively [11,12,13]. The gene discussed is EML4; the disease is lung carcinoma.